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二氧化硫对低氧性肺动脉高压大鼠肺小动脉内皮细胞炎性反应的影响 预览 被引量:13

Effect of Sulfur Dioxide on Small Pulmonary Artery Endothelial Cell Inflammation Reaction of Hypoxic Pulmonary Hypertensive Rats
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摘要 目的探讨外源性及内源性二氧化硫(SO2)对低氧性肺动脉高压(HPH)模型中炎性反应的影响。方法将Wistar大鼠随机分为4组:对照组(n=8)、低氧组(n=8)、低氧加SO2组(n=10,予外源性SO2供体Na2SO3/NaHSO3)和低氧加天冬氨酸异羟肟酸(HDX)组(n=10,予内源性SO2生成酶抑制剂HDX)。对低氧组、低氧加SO2组和低氧加HDX组大鼠予低氧处理21d,对照组大鼠置常氧环境。检测各组大鼠肺动脉平均压、肺组织匀浆中SO2水平,免疫组织化学法检测其肺小动脉内皮细胞核转录因子(NF)-κB和细胞间黏附因子-1(ICAM-1)表达情况。结果与对照组比较,低氧组大鼠肺动脉平均压升高127.13%(P〈0.01),其肺组织匀浆中SO2水平降低42.64%(P〈0.01),肺小动脉内皮细胞NF-κB表达阳性百分比升高303.47%(P〈0.01),ICAM-1表达升高119.25%(P〈0.01);与低氧组比较,低氧加SO2组大鼠肺动脉平均压降低15.09%(P〈0.05),肺组织匀浆中SO2水平升高40.54%(P〈0.01),内皮细胞NF-κB表达阳性百分比降低37.71%(P〈0.01),ICAM-1表达降低13.65%(P〈0.01);与低氧组比较,低氧加HDX组大鼠肺动脉平均压升高13.58%(P〈0.01),肺组织匀浆中SO2水平降低40.54%(P〈0.01),内皮细胞NF-κB表达阳性百分比升高22.18%(P〈0.01),ICAM-1表达升高11.92%(P〈0.01)。结论SO2在HPH炎性反应形成过程中发挥重要的保护性调节作用。 Objective To explore the effect of exogenous and endogenous sulfur dioxide ( SO2 ) on small pulmonary artery endothelial cell inflammation reaction in pathogenesis of hypoxic pulmonary hypetension ( HPH ). Methods Wistar rats were randomly divided into 4 groups : control group ( n = 8 ), hypoxic group ( n = 8 ), hypoxic plus SO2 group ( n = 10, given Na2 SO3/NaHSO3 ) and hypoxic plus hydroxamate (HDX) group (n = 10, given HDX). The rats of hypoxic group ,hypoxic plus SO2 group and hypoxic plus HDX group had been under a hypoxic condition for 21 days,while control group had been under room air. The mean pulmonary artery pressure ,the content of SO2 in lung tissue, the expression of nuclear factor - kappa B ( NF - KB ) and intracellular adhesion molecule - 1 ( ICAM - 1 ) were investigated and analyzed.-Resuits Compared with control group, mean pulmonary artery pressure of hypoxic group raised by 127.13 % (P 〈 0.01 ), the content of SO2 in lung tissue descended by 42.64% (P 〈0.01 ), the expression of NF - KB raised by 303.47% ( P 〈 0.01 ), and the expression of ICAM - 1 raised by 119.25 % (P 〈 0.01 ) ;whereas compared with hypoxic group, mean pulmonary artery pressure of hypoxic plus SO2 group descended by 15.09% ( P 〈 0.01 ), the content of SO2 in lung tissue raised by 40.54% ( P 〈 0.01 ), the expression of NF - KB descended by 37.71% ( P 〈 0.01 ), and the expression of ICAM - 1 descended by 13.65 % ( P 〈 0.01 ) ; compared with hypoxic group, mean pulmonary artery pressure of hypoxic plus HDX group raised by 13.58% ( P 〈 0.01 ), the content of SO2 in lung tissue descended by 40.54% ( P 〈 0.01 ), the expression of NF - KB raised by 22.18% ( P 〈 0.01 ), and the expression of ICAM - 1 raised by 11.92% ( P 〈 0.01 ). Conclusions SO2 play an important preventive role in protecting and regulating inflammation of experimental HPH in rats.
作者 田悦 美娜丽 刘雪芹 唐朝枢 杜军保 TIAN Yue ,Mainali ,LIU Xue - qin, TANG Chao - shu, DU Jun - bao (1. Department of Pediatrics, Peking University First Hospital, Beijing 100034, China; 2. Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100083, China;3. Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100083, China)
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2008年第13期 985-987,990,共4页 Journal of Applied Clinical Pediatrics
基金 国家长江学者奖励计划 国家杰出青年科学基金项目资助(30425010) 国家自然科学基金项目资助(30571971) 国家自然科学基金重点项目资助(30630031)
关键词 肺动脉高压 低氧性 二氧化硫 核转录因子-ΚB 细胞间黏附因子-1 大鼠 hypoxic pulmonary hypertension sulfur dioxide nuclear factor - kappa B intracellular adhesion molecule - 1 rat
作者简介 田悦,女,硕士生,研究方向为心肺血管疾病。 通讯作者:杜军保,男,主任医师,教授,博士生导师,研究方向为心肺血管疾病,电子信箱junbaodu@ht.rol.cn.net。
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